We evaluated the role of topical iganidipine on experimental aqueous flare elevation in rabbits. Transcorneal diffusion of prostaglandin E<sub>2</sub> (PGE<sub>2</sub>), 25 µg/ml or 7.09 × 10<sup>–2</sup> mmol/l, or highly selective agonists for prostaglandin E<sub>2</sub> receptor subtypes (EP), 25 µg/ml, was achieved with the use of a glass cylinder to produce aqueous flare elevation in pigmented rabbits. Iganidipine was topically administered before application of PGE<sub>2</sub> or EP agonists. Aqueous flare was measured with a laser flare cell meter. Topical instillation of 0.1% iganidipine once or twice inhibited 64 ± 8% (p < 0.01) and 84 ± 9% (p < 0.01) of PGE<sub>2</sub>-induced aqueous flare elevation, respectively. Two instillations of 0.1% iganidipine inhibited 95 ± 5% (p < 0.01) of EP2-agonist(ONO-AE1-259-01)-induced flare elevation and 98 ± 3% (p < 0.01) of EP4-agonist(ONO-AE1-392)-induced flare rise. Topical iganidipine may have anti-inflammatory activity in the eye.